Hrev_master [page 62] [Emergency Care Journal 2021; 17:9782] Emergency Care Journal 2021; volume 17:9782 Abstract We describe a rare complication of COVID-19 long after infection in a 76-years-old man presented to the Emergency Department with dyspnea and palpitations. A 12-lead Electrocardiogram (ECG) showed sinus tachycardia PR depression in the inferior leads associated with an apparent pseudo ST eleva- tion. In the absence of elevation of inflammatory indices, consid- ering the lack of symptoms neither NSAIDs nor colchicine were prescribed, and the patient was referred for clinical follow-up. After ten days ECG documented initial reduction of the widespread concave STE and PR depression, and the 1-month fol- low-up visit, the patient was asymptomatic with unremarkable physical examination, and a 12-lead ECG showed almost complete normalization of the ST and PR segments. Although pericardial involvement after COVID-19 infection has been already described, the incidence of subclinical pericarditis has not and may have implications for the monitoring of patients with uncomplicat- ed COVID-19 infection managed as outpatients. Introduction Cardiac complications of COVID-19 infection are emerging in the current pandemic, although few descriptions are available in those who are managed as outpatients.1 Notably, SARS-CoV2 can cause long-lasting illness, and the term long COVID describes the disease in people who continue reporting symptoms several weeks after the infection. Whether COVID-19 will become a chronic or permanent condition in some patients, and/or whether SARS-CoV- 2 infection might generate a new autoimmune disease (or autoim- mune-like) remains unknown.2 Case Report A 76-year-old white man without previous history of cardio- vascular disease entered the Emergency Department (ED) with dyspnea associated with palpitations. He denied other symptoms, and in particular chest pain. The patient referred a previous admis- sion 6 weeks prior, due to COVID-19 infection with initial signs of interstitial pneumonia, followed by clinical remission in 4 weeks. Since the nasopharyngeal swab SARS-CoV-2 RNA test was nega- tive 8 days before, quarantine was terminated. He reported long- term fatigue and paroxysmal nocturnal dyspnea. He was a non- smoker and he denied any substance abuse. His clinical history reported: primary systemic hypertension, Chronic Obstructive Pulmonary Disease (COPD), previous bladder cancer. Upon arrival at the ED, physical examination revealed blood pressure of 100/60 mmHg, heart rate of 120 bpm, oxygen satura- tion of 96% while breathing room air, and body temperature of 36.6 °C (he remained afebrile during the subsequent clinical course). Clinical examination Valid heart sounds without any murmur, normosphygmic peripheral arterial pulses, absence of peripheral edema and jugular distension, normal bilateral vescicular murmur. Arterial gas analysis pH of 7.46, oxygen partial pressure of 86.3 mmHg, carbon dioxide partial pressure of 33.1 mmHg with PiO2/FiO2 rate 435 mmHg. ECG A 12-lead Electrocardiogram (ECG) (Figure 1) showed sinus tachycardia at 120 bpm, with PR depression most evident in the Correspondence: Anna Giulia Falchi, Emergency Department, IRCCS Policlinico San Matteo, Piazzale Golgi 19, 27100 Pavia, Italy. Tel.: +39.0382.502039. E-mail: a.falchi@smatteo.pv.it Key words: Long covid; pericarditis; subclinical pericarditis. Contributions: All the authors contributed substantially to the concep- tion and design of the study, the acquisition of data, and the analysis and interpretation of data. All authors discussed the results and commented on the manuscript. Conflicts of interest: None. This work was not supported by any grant. Availability of data and materials: All data underlying the findings are fully available. Ethics approval and consent to participate: No ethical committee approval was required for this case report by the Department, because this article does not contain any studies with human participants or ani- mals. Informed consent was obtained from the patient included in this study. Consent for publication: The patient gave his written consent to use his personal data for the publication of this case report and any accompany- ing images. Received for publication: 25 March 2021. Revision received: 20 April 2021. Accepted for publication: 20 April 2021. This work is licensed under a Creative Commons Attribution 4.0 License (by-nc 4.0). ©Copyright: the Author(s), 2021 Licensee PAGEPress, Italy Emergency Care Journal 2021; 17:9782 doi:10.4081/ecj.2021.9782 Subclinical pericarditis long after SARS-CoV-2 infection: A case report Anna Giulia Falchi,1 Sergio Leonardi,2 Giovanni Cappa,3 Stefano Perlini1 1Emergency Department, IRCCS Policlinico San Matteo Foundation, Pavia; 2Coronary Care Unit and Laboratory of Clinical and Experimental Cardiology, IRCCS Policlinico San Matteo Foundation, Pavia; 3Emergency Medicine Postgraduate Training Program, University of Pavia, Italy Non -co mmerc ial us e o nly inferior leads associated with an apparent pseudo ST elevation. This finding was evident when the isolelectric line was identified as the TP segment (see red line). An ECG performed in the previ- ous month was normal. Chest radiography findings were unremarkable. Blood tests revealed normal levels of markers of myocyte injury [high-sensi- tivity troponin T level of 5 ng/L (double check), URL 49 ng/L], normal value of C-Reactive Protein (CRP) levels (0,57 mg/dL), normal blood cell counts. Transthoracic Echocardiogram (TTE) confirmed normal structure and function, with normal pericardium and no pericardial effusion. A nasopharyngeal swab specimen sam- ple was repeated, yielding negative results for SARS-CoV-2. Subclinical pericarditis was suspected. In the absence of inflammatory indices elevation, and considering the lack of symp- toms and the presence of renal insufficiency, neither NSAIDs nor colchicine were prescribed. The patient was referred for clinical follow-up at interval of ten days, in order to evaluate the clinical evolution. The absence of other causes for pericardial effusion and the history of recent COVID-19 infection with initial signs of inter- stitial pneumonia rose the suspicion of a viral etiology. It has to be underscored that the clinical manifestations in the post-acute peri- od after COVID-19 are largely unknown, considering that many of these features can resolve with time and their prevalence therefore depends on the evaluation moment. After ten days, concomitant with general clinical improve- ment, CRP was in the normal range, as well as TSH (0.33 mcU/L). ECG documented initial reduction of the widespread concave STE and PR depression (Figure 2). At the 1-month follow-up visit, the patient was asymptomatic with unremarkable physical examina- tion, blood pressure was 110/70 mmHg, and heart rate was 75 beats per minute. A TTE was repeated showing normal structure and function, and absence of pericardial effusion. A 12-lead ECG Case Report Figure 1. The 12-lead electrocardiogram showing sinus tachycardia at 120 bpm, with PR depression most evident in the inferior leads associated with an apparent pseudo ST elevation. Figure 2. The ECG after ten days documenting the initial reduction of the widespread concave ST and PR depression. [Emergency Care Journal 2021; 17:9782] [page 63] Non -co mmerc ial us e o nly showed almost complete normalization of the ST and PR segments (Figure 3). Acute pericarditis is the most common disease of the pericardi- um and is responsible for 0.2% of chest pain-related hospitaliza- tions, with an incidence two times higher in men than in women. Acute pericarditis is usually self-limiting, although it recurs in up to 30% of cases. In developed countries, viruses are the most com- mon causes, while Tuberculosis (TB) is the most common cause in the world and in developing countries, often associated with Human Immunodeficiency Virus (HIV) infection. In developed countries the most common causes of pericarditis are idiopathic or viral (42-49%). It is commonly diagnosed in viral infections, including coxsackie, enterovirus, herpes simplex, cytomegalovirus, H1N1, respiratory syncytial virus, parvovirus B19, influenza, varicella, HIV, rubella, echovirus, hepatitis B and C and finally for SARS-CoV-2.3-7 It is not always possible to define the responsible virus, and the viruses responsible in a given patient may be different genotypes of the same virus or different coexistent viruses. A post-acute COVID-19 syndrome was detected in a half of COVID-19 survivors, not limited to severe acute COVID19 patients, and with no identified predictors. Amenta et al.8 suggest that the post-acute period for COVID-19 starts 3 weeks after symptom onset. Also, they propose classifying post-acute manifes- tations into 3 categories: residual symptoms that persist after recovery from acute infection; organ dysfunction persisting after initial recovery; and new symptoms or syndromes that develop after initial asymptomatic or mild infection. A possible hypothesis for our patient is that after COVID-19 infection, virus-mediated damage to pericardial tissues keeps on, although with normal inflammation indices, probably by induction of pro-inflammatory cytokines, not included in our assessment. Although pericardial involvement after COVID-19 infection has been already described, the incidence of subclinical pericarditis has not and may have implications for the monitoring of patients with uncomplicat- ed COVID-19 infection managed as outpatients. References 1. Carfì A, Bernabei R, Landi F, et al. Persistent Symptoms in Patients After Acute COVID-19. JAMA 2020;324:603-5. 2. Moreno-Pérez O, Merino E, Leon-Ramirez JM, et al. Post- acute COVID-19 Syndrome. Incidence and risk factors: a Mediterranean cohort study. J Infect. 2021;S0163-4453(21) 00009-8. 3. Inciardi RM, Lupi L, Zaccone G, et al. Cardiac involvement in a patient with coronavirus disease 2019 (COVID-19). JAMA Cardiol 2020;5:819-24. 4. Fancello L, Monteil S, Popgeorgiev N, et al. Viral communities associated with human pericardial fluids in idiopathic peri- carditis. PLoS One 2014;9:e93367. 5. Linschoten M, Peters S, Van Smeden N, et al Cardiac compli- cations in patients hospitalised with COVID-19. Eur Heart J Acute Cardiovasc Care 2020;9:817–23. 6. Linschoten M, Asselbergs FW. CAPACITY-COVID: a European Registry to determine the role of cardiovascular dis- ease in the COVID-19 pandemic. Eur Heart J 2020;41:1795– 6. 7. Guo T, Fan Y, Chen M, et al. Cardiovascular implications of fatal outcomes of patients with coronavirus disease 2019 (COVID-19). JAMA Cardiol 2020;5:811-8. 8. Amenta EM, Spallone A, Rodriguez-Barradas MC, et al. Post- acute COVID-19: An overview and approach to classification. Open Forum Infect Dis 2020;7:ofaa509. Case Report [page 64] [Emergency Care Journal 2021; 17:9782] Figure 3. The 12-lead ECG after ten days showing almost complete normalization of the ST and PR segments. Non -co mmerc ial us e o nly